Etiology/Pathogenesis

Abstract

The pathogenesis of ALPE remains to be clarified. However, we propose the following hypothesis [4] (Fig. 61). Initially, anaerobic exercise such as a sprint may cause anaerobic glycolysis disorder of type II muscle fibers. Subsequently, adenosine 5′-triphosphate (ATP) deficiency may result in muscular injury. As a result, renal vasoconstrictive factors other than myoglobin may be released, promoting renovascular spasm at the interlobar/arcuate artery levels. However, for some reason, the grade of spasm may differ from branch to branch. The vascular spasm may induce acute tubular necrosis without increases in creatine phosphokinase (CPK) and serum myoglobin on the one hand, and renal angina with loin pain on the other. Risk factors for ALPE include renal hypouricemia, analgesic agents, and dehydration. However, vasoconstrictive factors remain to be clarified, and the involvement of muscle-derived substances and active oxygen is assumed. Furthermore, it is unclear why the grade of vascular spasm differs among the renal arterial branches, and at present there is no hypothesis to explain this.